Studies proposed in this application will investigate mechanisms by which the immune response of the host to IgE-secreting hybridoma cells results in specific regulation of IgE expression. My earlier studies have demonstrated that during in vivo passage in BALB/c mice, the IgE-- producing murine hybridoma B53 induces the development of effector cells in the host which in turn appear to regulate synthesis of IgE in the B53 cells by a mechanism that is dependent on the presence of host T lymphocytes. Suppression of IgE synthesis has been further demonstrated to be due to inhibition of epsilon-heavy chain transcription in the B53 cells. The aims of the present study are to investigate: 1) the host effector cells participating in and responsible for regulation of IgE synthesis in the IgE-producing hybridoma cells; and 2) the precise biochemical and molecular events that occur in the target hybridoma cells which result in regulation of IgE synthesis. These studies have the potential to identify the precise roles and basic mechanisms of host cells in regulating IgE immune responses. Such information would be highly relevant to studying immune responses in which IgE production leads to pathological consequences, such as anaphylaxis and atopic disorders.